Wednesday, April 14, 2010
Tuesday, April 13, 2010
Monday, April 12, 2010
2-aminoimidazole/triazole conjugate re-sensitizes multi-drug resistant strains of bacteria to the effects of conventional antibiotics...
We know that infections from antibiotic-resistant bacteria such as MRSA are especially difficult to get rid of because the bacteria can attach to surfaces and then create biofilms, sticky layers of cells that act as a shield and prevent antibiotics from destroying the bacteria underneath. While a limited number of existing antibiotics may destroy part of the biofilm, enough bacteria survive to create a recurring infection as soon as antibiotic therapy stops, and over time the surviving bacteria build resistance to that antibiotic. Though I have covered some recent developments in the MRSA field, the following findings are really interesting for me...
Now researchers lead by Dr. Christian Melander, from North Carolina State University have found that, 2-aminoimidazole/triazole conjugate will re-sensitize multi-drug resistant strains of bacteria to the effects of conventional antibiotics (including MRSA and multi-drug resistant Acinetobacter baumannii), apart from the synergistic effect between the conjugate and antibiotics toward dispersing pre-established biofilms.
Melander and his team, in collaboration with NC State biochemist John Cavanagh, found that pre-treating the bacteria with their compound and then introducing the antibiotic penicillin one hour later increased the penicillin's effectiveness 128-fold, even when the bacteria was penicillin resistant. The antibiotics also provided a 1,000-fold enhancement to the ability of the 2-aminoimidazole to disperse biofilms.
Researchers conclude that, compound cooperates with conventional antibiotics, overcoming an infectious threat that would otherwise persist if treated with either agent individually.....
Ref : http://aac.asm.org/cgi/content/abstract/AAC.01418-09v1
Sunday, April 11, 2010
Minocycline - Effective defense against HIV ?
We know that Minocycline hydrochloride, also known as minocycline (structure), is a broad spectrum tetracycline antibiotic, and has a broader spectrum than the other members of the group. It is a bacteriostatic antibiotic. It is primarily used to treat acne and other skin infections as well as lyme disease. It may be used to treat certain strains of MRSA infection and disease caused by drug resistant Acinetobacter. Its also used in DMARD (Disease-Modifying Anti-Rheumatic Drug) for RA.
Now, Johns Hopkins scientists have found that this safe and inexpensive antibiotic (minocycline), effectively targets infected immune cells in which HIV, the virus that causes AIDS, lies dormant and prevents them from reactivating and replicating.
As per the claim by the researchers, minocycline, likely will improve on the current treatment regimens of HIV-infected patients if used in combination with a standard drug cocktail known as HAART (Highly Active Antiretroviral Therapy). Though HART is really effective in keeping down active replication, minocycline is another arm of defense against the virus.
Dr. Janice Clements lead researcher claims that, unlike the drugs used in HAART which target the virus, minocycline homes in on, and adjusts T cells, major immune system agents and targets of HIV infection. and minocycline reduces the ability of T cells to activate and proliferate, both steps crucial to HIV production and progression toward full blown AIDS.
The idea for using minocycline as an adjunct to HAART resulted when the Hopkins team learned of research by others on rheumatoid arthritis patients showing the anti-inflammatory effects of minocycline on T cells. Interestingly the same researchers earlier found that minocycline treatment had multiple beneficial effects in monkeys infected with SIV, the primate version of HIV. In monkeys treated with minocycline, the virus load in the cerebrospinal fluid, the viral RNA in the brain and the severity of central nervous system disease were significantly decreased. The drug was also shown to affect T cell activation and proliferation.
The team used molecular markers to discover that minocycline very selectively interrupts certain specific signaling pathways critical for T cell activation. However, the antibiotic doesn't completely obliterate T cells or diminish their ability to respond to other infections or diseases, which is crucial for individuals with HIV. Researchers conclude that, this new understanding about minocyline's effects on a T cell might help to find even more drugs that target its signaling pathways.
At Johns Hopkins and elsewhere, scientists are now testing whether giving HIV patients minocycline benefits them, let us hope for the positive results....
Ref : http://www.usnews.com/science/articles/2010/03/26/existing-antibiotic-might-help-keep-wraps-on-aids-virus.html
Saturday, April 10, 2010
UT Southwestern researchers find clues to TB drug resistance.....
In continuation of my update on TB and its challenges...
Now researchers from the University of Texas Southwestern Medical Center at Dallas, have come up with some interesting info. i.e., a type of blood pressure medication shows promise at overcoming some drug-resistant tuberculosis, at least in the laboratory.
Dr. Gumbo (lead researcher) and his colleagues used an experimental apparatus to simulate the way TB bacteria grow in the human lung. When they exposed the bacteria to drugs commonly used to treat the disease (ethambutol and isoniazid), the bacterial cells activated a cellular mechanism that pumps each drug out of the cells.
"The pumping action enables the rapid emergence of high-level resistance to the drugs whether administered together as well as individually, Dr. Gumbo said".
As per the claim by the researchers, resistance was drastically reduced when the researchers gave the blood-pressure drug reserpine – which is known to block this pumping action – to the TB cells before administering ethambutol and isoniazid.
Researchers now want to test all the first-line drug treatments together with the pump blocker in humans. Hope they will come up with positive results.....
Researchers now want to test all the first-line drug treatments together with the pump blocker in humans. Hope they will come up with positive results.....
Ref : http://www.utsouthwestern.edu/utsw/cda/dept37389/files/582308.html
Thursday, April 8, 2010
Telaprevir-based regimens increase rates of SVR in patients with genotype 1 HCV infection
In continuation of my update on telaprevir-based regimens, I found this article interesting to share with.....
In a clinical trial known as PROVE 3 published in this week's New England Journal of Medicine, treatment with telaprevir-based regimens significantly increased rates of sustained viral response (SVR) in patients with genotype 1 hepatitis C virus (HCV) infection who did not achieve SVR with at least one prior course of pegylated-interferon and ribavirin therapy. In the trial, 51 percent and 53 percent of patients who received telaprevir in combination with pegylated-interferon and ribavirin as part of a 24-week or 48-week regimen, respectively, achieved SVR. More...
Scientists show carbon nanotubes can be broken down by MPO
Carbon nanotubes were once considered biopersistent in that they did not break down in body tissue or in nature. In recent years, research has shown that laboratory animals exposed to carbon nanotubes via inhalation or through injection into the abdominal cavity develop severe inflammation. A combined study by a team of Swedish and American scientists have come up with an interesting finding, which will be a breakthrough in nanotechnology and nanotoxicology. As per the claim by the researchers, "endogenous MPO can break down carbon nanotubes". This enzyme is expressed in certain types of white blood cell (neutrophils), which use it to neutralise harmful bacteria. Now, however, the researchers have found that the enzyme also works on carbon nanotubes, breaking them down into water and carbon dioxide. The researchers also showed that carbon nanotubes that have been broken down by MPO no longer give rise to inflammation in mice. More....
Scientists show carbon nanotubes can be broken down by MPO
Tuesday, April 6, 2010
Saturday, April 3, 2010
Thursday, April 1, 2010
New anti-inflammatory drug shows promise for treating inflammatory disorders
In one of my earlier blog, I did mention about the antiinflammatory activity of H2S gas. Now interestingly John Wallace, a pharmacologist and director of the Farncombe Family Digestive Health Research Institute at McMaster University, compared naproxen, a commonly used NSAID, to a novel anti-inflammatory drug, ATB-346 (ATB-346 is a derivative of naproxen which releases hydrogen sulfide), which he developed in collaboration with a team of Italian chemists and is now commercializing through his company, Antibe Therapeutics Inc. The basis for this research is by the fact that hydrogen sulphide is an important mediator of gastric mucosal defence. As we all know the ulcerogenecity associated with NSAIDs, there is a need to have NSAIDs with least or no ulcerogenecity.
As per the claim by the researchers, ATB-346, [above, structure : 2-(6-methoxy-napthalen-2-yl)-propionic acid 4-thiocarbamoyl-phenyl ester] acts by inhibiting cyclooxygenase-1 and 2 and reduces inflammation (in vivo). More interesting out come from their research is that ATB-346 suppressed gastric prostaglandin E2 synthesis as effectively as naproxen, but produced negligible damage in the stomach and intestine.
ATB-346 did not cause significant damage, where as naproxen rendered significant gastric mucosa damage (e.g. ablation of sensory afferent nerves, inhibition of endogenous nitric oxide or hydrogen sulphide synthesis, co-administration with aspirin, antagonism of KIR 6.x channels). Unlike naproxen and celecoxib, ATB-346 accelerated healing of pre-existing gastric ulcers. In a mouse airpouch model, ATB-346 suppressed cyclooxygenase-2 activity and inhibited leukocyte infiltration more effectively than naproxen. ATB-346 was as effective as naproxen in adjuvant-induced arthritis in rats, with a more rapid onset of activity, but with substantially reduced gastrointestinal toxicity (100 times safer than naproxen). Unlike naproxen, ATB-346 did not elevate blood pressure in hypertensive rats.
The researchers concluded that H2S-releasing NSAIDs appear to represent a promising alternative to existing therapies for the treatment of inflammation and pain. Future research will focus on the potential cardiovascular benefits of these drugs. .....
Ref : John L Wallace et. al., British Journal of Pharmacology, 159(6), 1236 - 1246
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